Abstract
Headache associated with acute sinusitis is a widely accepted entity; diagnosis can be made by the associated nasal symptoms and computed tomography (CT) or endoscopic findings. However, chronic sinusitis as a cause of headache or facial pain is still controversial. In a few cases with sinus headaches may not necessarily present with a typical sinusitis history. Thus, referred headache of rhinogenic origin, in the absence of sinonasal symptoms, usually delays its diagnosis. Here we report two patients who presented with primary headache syndrome without significant nasal or sinus symptoms and who failed to respond to medical therapy.
Case reports
Case 1
A 56-year-old female was referred to us by a neurologist; she had a 5-year history of chronic headache and had had exacerbations in a recent 2-week period. The pain was initially located in the frontal and right temporal area and then extended to her right cheek, occipital area and posterior neck. She also described right shoulder pain and right arm tingling and a numbness sensation when the headache attacked. The pain attacks occurred once to twice a month, each episode lasting 3–4 days. There were no phono/photophobia or autonomic symptoms. She had no history of any sinusitis or other sinus problems and also denied sinonasal symptoms such as nasal discharge, postnasal drip and nasal congestion accompanying headache. During the past 5 years she had controlled her head pain by using analgesics bought at a pharmacy.
Over the previous 2 weeks she had begun to experience increased severity and frequency of pain attacks and did not respond to analgesics as usual. Various drugs prescribed by the neurologist in the past 2 weeks had also failed to produce any therapeutic effect. She was referred to our department for evaluation of continuous severe headache.
On examination, rigid endoscopy showed no intranasal abnormalities, but sinus CT revealed increased soft tissue density in the right posterior ethmoid sinus (Fig. 1). Following a tentative diagnosis of sinus headache, empirical oral antibiotics were given for 1 week for her sinusitis but achieved no response.
(a)Axial computed tomographic (CT) scan shows surrounding bone is thickened (arrow). (b) Coronal CT of paranasal sinuses shows opacification in the right-side posterior ethmoid sinus (∗).
Because of the lack of response to conservative medical treatment, functional endoscopic sinus surgery was performed after admission. The final pathological report showed aspergillosis. One month after endoscopic sinus surgery, her headache became milder and infrequent and did not recur during the follow-up period of 18 months.
Case 2
A 26-year-old female with no previous history of headache or migraine came to our out-patient department because of severe headache attacks for 3 months. She had received treatment at a local medical clinics but without any relief. She stated the headache attacks were strongly in the right-sided frontal and parietal areas. The pain attacks occurred two to three times a week and lasted for 1–2 h. No other accompanying symptoms such as nasal obstruction, purulent nasal discharge or lacrimation were noted during the attacks. Office nasal endoscopic examination was performed and revealed a fungal ball in the right-sided superior meatus. CT scan showed only soft-tissue opacity in the right-sided posterior ethmoid sinus (Fig. 2).
(a) Axial computed tomographic (CT) scan shows surrounding bone is thickened (arrow) without bony destruction. (b) Coronal CT of paranasal sinuses showed opacification in the right-side posterior ethmoid sinus (∗).
She received endoscopic sinus surgery with adequate sinus drainage and complete removal of the suspected fungal ball; the pathology report showed aspergillosis. Her head pain improved at 1 week postoperatively. The patient has since been headache free, with a follow-up of 1 year.
Discussion
The precise mechanism by which fungal sinusitis occurs is still unknown. It might theoretically develop when fungi enter the sinus and provide soluble antigens or irritants that increase mucosal inflammation and physically obstruct the sinus ostium, leading to episodes of acute sinusitis. Facial pain, pressure or headache are common but clinical symptoms may not be useful in differentiating fungal sinusitis from bacterial sinusitis.
Both fungal and bacterial sinusitis-related headache can mimic primary headache syndromes. Ninety percent of patients experienced sinus headaches that fulfilled the International Headache Society (IHS) criteria for migraine (1). The IHS recommendations also suggest that it is easy to confuse migraine and tension-type headache, with headache attributed to sinusitis because of similarity in the location of the headache (2). Thus, in patient with headache caused by relatively small sinus lesions without nasal symptoms, the diagnoses are more difficult.
Recent studies have demonstrated that substance P is likely to be a mediator of pain in the nose or paranasal sinuses. It mediates pain impulses to the cortex via afferent C fibres. Together with this orthodromic impulse, an antidromic impulse can start releasing substance P to local effector cells in the mucosa causing plasma extravasation, vasodilation and hypersecretion. These simultaneous orthodromic and antidromic impulses cause an axon reflex and may explain why an initially relatively small localized lesion can lead in a vicious cycle to severe symptoms (3, 4). Unlike the usual facial pain area (behind and around the eyes or in the occipital area) (5) that ethmoid sinusitis involves, the principal complaints of our patients were hemifacial pain and pain in the occipital area and posterior neck with radiation to the shoulder and arm. Paraesthesia of the arm was also noted during every episode of headache. The possible origin of this symptom is the trigeminal nerve. Sensory inputs from trigeminal three divisions and upper cervical sensory innervating structures in the neck and shoulders have synapse in the trigeminal brainstem sensory nuclear complex (6, 7). However, these convergences and sensitization might not be restricted to these complex neurons. Recent experimental and clinical data suggest that thalamic neurons may be involved (8, 9). The involvement of thalamic neurons may explain why cutaneous allodynia and hypersensitivity sometimes spread to dermatomes outside the primary innervation areas of trigeminocervical neurons (10).
The neurobiology of migraine and primary sinonasal pain share some of these trigeminal pathways. Migraine aura can also present with these fully reversible sensory symptoms. In case 1, although posterior ethmoid sinus lesion was detected by CT imaging, we can not exclude the possibility of coexistence of migraine and sinus headache. However, her headache became infrequent immediately after surgery and did not recur during follow-up. This suggests that either her intractable headache was induced by minimal sinus disease or minimal sinus disease served as a trigger for migraine attacks.
Migraine can present with concomitant rhinosinusitis and vice versa and create a confusing clinical picture. Otolaryngologists need to consider a diagnosis of migraine; equally, neurologists need to consider the possibility that a patient's headaches are of rhinogenic origin (11). Nasal endoscopy or CT of paranasal sinus can disclose evidence of sinusitis. Disappearance of headache after remission or successful treatment of acute sinusitis also can help to differentiate sinus headache from primary headache.
In conclusion, sinus headache is often confused with primary headache such as migraine or tension-type headache. Coexistence of those common primary headaches and sinusitis is possible and reminds us that finding one cause for headache dose not exclude other simultaneous headache disorders (12). Thus, complete rhinological work-up may be warranted in the chronic headache patient who is refractory to conventional medical therapy.